Sports commentators love to describe explosive athletes as “made up of quick-twitch”. And while that’s certainly true, it’s not particularly helpful because so do the rest of us. That’s right, from elite ultra-marathoners to the slowest, least athletic humanoid on the planet – we’ve all got plenty of “fast-twitch” (FT) fibers in our muscles. As a scientific team whose primary research focus involves studying individual muscle fibers for their “type” across a wide spectrum of athletes (e.g., UFC fighters, world-caliber powerlifters and weightlifters, Olympic champion sprinters, to 90+ yr old record holding cross country skiers (30), etc.), nothing makes us feel like we’re covered in carbuncles more than hearing people spew falsities about the nature of human skeletal muscle fiber types.

The most perpetuated myth is that fiber type can’t change with training. Many versions of this mistake exist: you can’t change at all, or you can, but only from FT to slow-twitch (ST), or you lose the super-fast twitch (SFT) when you train. etc. etc. etc.

Don’t feel bad if you’ve made any of these mistakes, most scientists (who don’t specifically study human fiber types) are still pretty confused (33). But enough if you want to know the truth, we’ve provided a condensed version here. If you really want to get after it, top off your coffee or yerb mate tea and hop over to https://www.youtube.com/watch?v=qpqiwKYQFHg for the 3 hr video version, or listen to the first episode (Volume 1, Chapter 1) of my podcast/mini-documentary series “The Body of Knowledge” (iTunes, Stitcher, etc.).

What Does “Fast-Twitch” and “Slow-Twitch” Even Mean?

Muscle fibers use two filaments (actin and myosin) to produce movement: a myosin grabs actin and pulls it towards the midline, thus shortening and stacking filaments (see sliding filament theory). We call this a muscle contraction (or “twitch”). The faster this occurs, the fast the muscle contracts, the faster you move. The speed contraction is regulated by an enzyme known as ATPase (remember this for later), which sits on the head of the myosin. The contractility of muscle fibers exist across a wide continuum from slow to fast, but to make things easy, we put them into crude categories called “types”. FT fiber types usually contract with more velocity, but fatigue much quicker; the inverse being true of ST types. In fact, FT produce 5-6x more power than ST while SFT produce ~20x more power than ST (7).

Work in the 1660’s by Neil Stenson (1667) & Stefano Lorenzini (1678) showed scientist clearly understood the functional differences between types (“red vs. white” fibers). Yet, it wasn’t until 1965 that we realized the contractile velocity was a function of the ATPase “type”, and this could easily be measured in the lab with a test called “histochemistry” which makes the fiber turn either black or white (depending on type) (5). The problem was while some fibers were a distinct black or white (Figure 1), most were actually various shades of grey (Figure 2). With only two category options (FT or ST), each scientist was forced to arbitrarily which grey fibers to call “white”, and which to call “black”.

This subjectivity lead to an avalanche of research over the next 40+ years that exacerbated confusion and resulted in numerous nomenclature changes. It got so bad that in 1971 Guth and Yellin questioned the futility of the “so called fiber types”, stating “fiber types are simply too dynamic and flexible” to bother categorizing (16). However, in 1986 a new measurement technique (SDS-PAGE) allowed much more accurate (1) measurement of fiber type by analyzing each fiber individually based on the molecular weight of the myosin heavy chain (MHC), not the ATPase (9). By 1988 it was acknowledged that human skeletal muscle is comprised of 3 “pure” (MHC I, MHC IIa,MHC IIx) and 3 “hybrid” (MHC I/IIa, MHC IIa/IIx, and MHC I/IIa/IIx) types (6). The hybrids are single fibers that are two (or 3) fiber types simultaneously (Figure 3).

By the mid 1990’s gene analysis studies from multiple laboratories confirmed the SFT is NOT “IIb”, but rather IIx (hence some old books refer to it as IIb, erroneously) (29). It was also quickly realized that pure MHC IIx are extraordinarily rare, occurring in <1/1000 fibers (or 0.1%) (1, 4, 13), and what most scientists thought were MHC IIx were actually MHC IIa/IIx fibers misclassified as MHC IIx (4, 17).

Do They Change with Training?

The fiber type percentage (FT%) differs massive from person to person, and from muscle to muscle (see our newest paper on FT% asymmetries between the dominant and non-dominant limb – in press). The physiological capacity for a muscle fiber to change type is beyond reproach, with hundreds (if not thousands) of studies across multiple disciplines (3, 13, 25), dating back to the 1960’s (8), as evidence. However, it wasn’t until Dr. Reggie Edgerton’s famous 1969 study the question was addressed in response to exercise training in normal healthy mammals (in this case, mice) (10). A few years later Gollnick and colleagues performed the first human trial and reported no change in FT% following endurance training (15). Several studies followed with similar conclusions until Andersen & Henriksson reported a significant shift from IIx to IIb, and no change in I (2) (remember these are now know to actually be IIa/IIx fibers, not IIx…). An epic study the very next year saw the ST fibers convert to FT following 6 weeks of “anaerobic training”, and revert right back to ST after the training then changed to “aerobic” (19). The field stumbled along with apparent conflicting reports (more on this in the “Why the Confusion” section…spoiler, they don’t actually conflict) the next ~40 years, and while many details remain unresolved (see “Holes in the Fiber Type Science” section) a general consensus exists among scientists who actually work in this area regarding fiber type changes with exercise:

All fiber types change with training, and it happens quickly.

Most sedentary people have ~20-40% of their fibers at hybrids. Active people are usually in the 10-20% range. Very highly trained athletes may have little to no hybrids.

Extremely plasticity exists (i.e., it’s easy to change) between all fiber types, though pure MHC I appear more rigid (but they still do change).

The amount of change is controlled by exposure time and intensity; training more often = more change.

For example, our recent study (in review) on monozygous twins (i.e., exact same DNA) with 30+ years of differing exercise routines showed MHC I FT% of 90%+ in the endurance exercising twin to only ~40% in the sedentary one.

A 10% or more change in FT% would be reasonable after a few months of training.

See this article for the most complete review on FT% shifting in human skeletal muscle with changes in physical activity.

Why the Confusion?

There actually isn’t as much controversy with this topic as one thinks. In fact, at last count >25 studies have implemented the single fiber SDS-PAGE approach, and they’re all in relative agreement. However, the less specific histochemistry technique routinely yields conflicting findings. As does a method known as SDS-PAGE homogenate (in which the entire muscle sample is analyzed collectively – instead of one muscle fiber at a time). Both histo and homogenate have the same issue: neither are able to measure the hybrids. This leads to numerous errors in classification – particularly of MHC IIa/IIx fibers.

Picture these 2 examples.

Example 1: A study analyzes whether or not FT% changed after 10 weeks of heavy strength training in recreationally active college males. They use histo and find the group average before was 50% I and 50% IIa, and these percentages did NOT change after the training. What happened? Remember, since they couldn’t analyze hybrids, likely 10-20% of those fibers were arbitrarily assigned as either pure I or pure IIa. Thus, their true FT% probably looked something more like 45% MHC I, 10% MHC I/IIa, 35% MHC IIa, and 10% MHC IIa/IIx. When they trained for the 10 weeks, 5% of the MHC I/IIa converted to MHC I (not enough to be “statistically significant”) and the other 5% to MHC IIa, and all 10% of the MHC IIa/IIx converted to MHC IIa. Thus, the massive change in FT% is completely missed. How could you ever find a FT% when the method can’t measure the fiber types most responsive to changes in physical activity? You can’t. Hence, decades of confusion.

Example 2: Let’s say the same study used homogenate, which can measure MHC IIx, but not hybrids. The problem: the inability to measure hybrids means the MHC IIa/IIx fibers are actually misidentified as pure MHC IIx fibers (remember, these are almost completely absent in health humans). So say he group FT% before was 50% I, 35% IIa, and 15% IIx. After the 10 weeks, the findings show a FT% of 55% I, 45% IIa, and 0% IIx (FYI, this is exactly what you’ll read in most modern textbooks). But the participants didn’t actually “lose SFT IIx” fibers, because they never had them to begin with. Just like in example 1, the misclassified hybrids cause erroneous conclusions about the nature of FT% changes with training.

Pay attention to the measurement methods next time you read a FT study, and I bet you’ll start seeing the pattern.

Holes in the Fiber Type Science.

While the case is close on “whether or not FT% change with training”, many questions about the details remain. In fact, a recent study from our lab suggests that while a negative relationship may exist between fatigue and the amount of FT fibers in untrained individuals, it may not in strength-trained men. Remember, many physiological factors go into force production. FT% is simply one, and can only explain a small portion of physical performance (4).

We don’t know much about athlete FT% in general, and virtually nothing about anaerobic athletes, specifically. To date, only 29 experiments have tested the vastus lateralis (the most common muscle to biopsy) of male athletes from power sports: judo (1x), soccer (2x), volleyball (1x), sprinters (8x), throwers (3x), bodybuilders (6x), powerlifters (4x), and “Olympic” weightlifters (WL) (4x). Unfortunately, these studies assessed an average of only 7.8 subjects. Several used ≤2, and only 6/29 obtained double digit sample sizes. Only 2 used single fiber SDS-PAGE.

The first found that bodybuilders (n = 8) contained more MHC I/IIa, MHC IIa than age matched physical education students; and MHC IIx were completely absent (21). The other was the only study ever to performed single fiber SDS-PAGE on an elite speed, strength, and/or power athlete found a world record holding sprinter Colin Jackson had an ASTONISHING 24% MHC IIx (video here)(31). How is this possible?! We don’t have a clue. Makes you wonder what would happen if people did biopsies on more people like this….

Women? Forget about it.

Only 8 studies have examined female athletes FT%: field hockey (n=5), divers (n=4), orienteers (n=7), track and field (n=6), judo (n=4), bodybuilders (n=4), endurance cycling (n=19), and tennis (n=15). In other words, in 50+ years of research and available technology, only 71 female athletes, from 8 different sports (~9 per sport) have ever been fiber typed, with almost half coming from two studies.Only 10 total strength and speed female athletes have been fiber typed. Only 6 of these women, a group of collegiate track & field sprinters, jumpers, and throwers, were measured with single fiber SDS-PAGE (28).

Our lab is doing everything in our power to change this, but funding for studies like this is virtually impossible, and at an all-time low. We’re trying like crazy to collect biopsies from as many top athletes competing at 2017 IWF World Championships and the American Open Finals as both are right down the street from our lab, but it’s tough going. Let’s hope for the best.

The limited evidence indicates females have more slow-twitch fibers than men (26), and single fiber contractile force and velocity adaptations vary between men and women in a fiber type-dependent and MHC-specific manner (23). This all seemingly indicates a need for development of fiber type and gender-specific training programs. Newer studies have attempted this, but opted to use genetic targets (alpha-actinins) which code for fast-twitch fibers, in place of direct FT% measurement (20). However, phenotypical expression is a result of both genotype and external stimuli, leading researcher to conclude that alpha-actinis do not play a significant role in determining adult FT% (26). This probably explains why some studies find correlations between certain genotypes and success in power sports (22), but others do not (14). Thus, while genetic targets are an exciting forefront and highly scalable, they do not appear appropriate as a surrogate of FT% and fail to fill the outlined knowledge gaps.

We also don’t know really anything about which rep ranges, periodization styles, volumes, intensities, or otherwise induce which specific FT% changes. Concurrent/cross-training? No data. Think about it. The vast majority of sports: gymnastics, football, baseball, basketball etc. all have zero studies. We know diet and certain micronutrients can change FT% in other mammals, so it would be silly to think it doesn’t happen in humans also (24). Solid evidence has already shown differential shifts in FT% in response to long-term high sugar/high fat diets with and without resveratrol supplementation in primates (18). Hell, even carbon dioxide concentrations alter FT% (27), suggesting a need for extensive study of interventions like ice baths, saunas, cryotherapy, high altitudes, and zero gravity. And don’t even get started on things like ethnic backgrounds…

Conclusion

What should you do to ensure your training optimizes your FT%? We don’t really know. Any other answer is a straight lie. Our best guess: if you want to make more FT fibers, train fast and heavy. Better endurance? Practice getting tired. Maximize growth? Do a combination of high volume/low intensity with low volume/high intensity lifting. At least, this is the best we know as of now.

So while we’ve got countless more questions than answers at this point, we can comfortably say that not only do human skeletal muscle fiber types change, but it happens often, quickly, and in response to just about everything you do.